Chikungunya (CHIK) virus has the ability to cause explosive epidemics in Africa, India, and southeast Asia (Epstein, 2007; reviewed by Powers and Logue, 2007). The virus is transmitted by mosquitoes of genus Aedes (Ae.). CHIK virus has been responsible for unprecedented magnitude outbreaks in Reunion Island and Indian Ocean since 2005, and in India where an estimated 1.4 million inhabitants have been infected in 2006 (Schuffenecker et al., 2006; Staikowsky et al., 2006; Arankalle et al., 2007; reviewed by Pialoux et al., 2007).
Humans infected with CHIK virus typically experience acute illness with incapacitating polyarthralgia, severe muscle pain and stiffness in the joints sometimes followed by a maculopapular rash (Johnston and Peters, 1996; Borgherini et al., 2007; reviewed by Pialoux et al., 2007; Rulli et al., 2007). CHIK virus infection is associated in almost all cases with myalgias. CHIK virus infection of satellite cells within the muscles could explain, in part, some features of clinical manifestations (Ozden et al., 2007). The clinical symptomes of Chikungunya virus infection are often misdiagnosed for arboviral diseases due to other arthritogenic alphaviruses such as Igbo-Ora virus from Western Africa, O'nyong-nyong (ONN) virus from Central Africa, Ross River and Barma viruses from Australia and the Pacific, Mayaro virus from South America, and cosmopolitan Sindbis (SIN) virus.
CHIK virus is a member of the genus Alphavirus and family Togaviridae (reviewed by Strauss and Strauss, 1994). The alphaviruses are small enveloped single—stranded positive RNA viruses exhibiting a large cell tropism. The viral surfaces are covered in membrane-anchored spikes composed of triplets of heterodimers of the envelope E1 and E2 glycoproteins. The viral spike proteins facilitate attachment to cell surfaces and viral entry. The E1 envelope glycoprotein is a class II fusion protein that mediates low pH-triggered membrane fusion during virus infection. E2 is a 50 kDa type I transmembrane glycoprotein: the first 260 amino acids constitute the ectodomain, followed by about 100 amino acids that form the stem region, a spanning region of 30 amino acids, and a short cytoplasmic endodomain of 30 amino acids (Pletnev et al., 2001; Mukhopadhyay et al., 2006). pE2 (the 62-kDa precursor to the E3 and E2 proteins) and E1 are assembled as heterodimers in the endoplasmic reticulum (reviewed by Strauss and Strauss, 1994). After the cleavage of pE2 in the Golgi apparatus to form E3 and E2, the E1-E2 complexes are transported to the plasma membrane (PM). The interaction of the cytoplasmic E2 endodomain with the preassembled nucleocaspid is one of the initial steps in the process of virus envelopment at the PM. Integrity of virion is maintained by direct interactions between E1 and E2 (Strauss and Strauss, 1994). During the course of alphavirus life cycle, the E2 glycoprotein is responsible for receptor binding. Most neutralizing antibodies recognize epitopes in E2 rather than E1 (reviewed by Strauss and Strauss, 1994). Antibodies that recognize conformational epitopes on the outer surface of E2 have the potential to neutralize alphavirus infection.
Biological diagnosis of CHIK virus infection is essentially based on quantitative real-time RT-PCR-based method during the initial viraemic phase (Edwards et al., 2007; Laurent et al., 2007; Santhosh et al., 2007). Serological methods detect anti-CHIK IgM early times after the first clinical manifestations and specific IgG after two weeks (reviewed by Pialoux et al., 2007). However, ELISA and immunodetection assays are poorly specific and sensitive due the cross reactivity of CHIK virus with related members of the Semliki Forest (SF) antigenic complex (Greiser-Wilke et al., 1991).